Parental Diet Exposure and High-Sugar-Fat Intake Effect on Glucose, Triglyceride and Cholesterol Hemolymph Level of <i>Drosophila melanogaster</i> across Five Generations

In HIV-infected individuals, hypertriglyceridemia was first reported in the absence of antiretroviral therapy, and was probably dependent on the unregulated production of cytokines such as IFN-α or tumour necrosis factor alpha [1]. Among patients receiving highly active antiretroviral therapy (HAART), approximately 60–70% eventually develop hypertriglyceridemia, often associated with a complex syndrome of lipodystrophy, central adiposity and insulin resistance [2]. Moreover, pancreatitis and premature cardiovascular complications have been reported in HIV-infected patients with HAART-related hypertriglyceridemia [3,4]. Several therapeutic approaches to HIV- or HAART-related hypertriglyceridemia have been suggested or evaluated in small groups of patients. In AIDS patients, in the absence of antiretroviral therapy, l-carnitine treatment resulted in a strong reduction of serum triglyceride levels [5]. This was explained by the effect of l-carnitine on tumour necrosis factor alpha modulation. In patients with HAART-related hypertriglyceridemia, low l-carnitine doses (2 g/day) for 12 weeks had no significant effect on triglyceride levels but a trend was noted for decreased cholesterol levels [6]. Favourable results have been reported for gemfibrozil [7], bezafibrate [8], and fenofibrate [9]. On the other hand, the statins infrequently normalized cholesterol and triglyceride levels in patients with protease-inhibitor-related hyperlipidemia and might have increased hepatic toxicity [10]. We conducted a prospective open trial in 16 adults (one woman, 15 men) aged 44.1 ± 9.3 years, with HIV infection known for 8.8 ± 3.8 years (range 2–14), who had been receiving antiretroviral agents for 7.2 ± 2.8 years (range 2–12). Their ongoing HAART included at least one protease inhibitor in all but one patient. l-Carnitine, 3 g a day, was administered orally for 8.9 ± 5 months (range 2.3–19). Fasting serum triglyceride levels, cholesterol, glucose, C-peptide, other metabolic and biochemical parameters, CD4 cell counts and HIV-RNA levels were measured at 1–2 month intervals. Baseline data were compared with results at month 1, month 2, at the first change of HAART (after initiating l-carnitine therapy), and at the end of therapy or the time of data analysis. Changes in mean triglyceride, cholesterol and glucose levels from baseline were analysed using Student's t-test; a two-sided P value less than 0.05 was considered significant. At baseline, the viral load was 3.4 ± 1.5 logs (range < 1.7–5.27) HIV-1-RNA copies/ml, and the median CD4 cell count was 218 ± 210 cells/ml (range 0–670). Mean baseline triglyceride levels were 5.67 ± 1.78 mmol/l (range 2.28–8.74; normal 0.5–2.0), cholesterol levels were 5.6 ± 1.58 mmol/l (range 3.43–8.07; normal 2–5.2), and glucose levels were 5.3 ± 0.93 mmol/l (range 3.7–7.4; normal 3.6–6.1). In comparison with baseline values, during l-carnitine therapy, triglyceride levels were decreased by 39% at month 1, by 28% at month 2, by 23% when HAART was first changed, and by 34.7% at the last measurement (Table 1). The reduction in triglyceride levels was statistically significant at every time-point. A normal triglyceride level of 2.3 mmol/l or less was recorded in 15% of patients after 2 months of therapy, and in 40% of patients at the last evaluation. However, near-normal triglyceride levels (≤ 3 mmol/l) were obtained in 54% of patients after 2 months of treatment, and in 69% at the last assessment. No significant effect was noted for cholesterol (Table 1) and C-peptide in this group of patients.Table 1: Effects of l-carnitine on triglyceride and cholesterol levels. The role of carnitine in the regulation of fatty acid and carbohydrate metabolism is very complex. It is an essential co-factor for the transfer of fatty acyl groups into the mitochondrial matrix, where they undergo beta-oxidation [11]. Carnitine also plays a role in the transfer of acetyl and other short acyl groups from peroxisomes to mitochondria for further oxidation [11]. In conclusion, in this pilot trial, l-carnitine at a daily dose of 3 g significantly decreased serum triglyceride levels in HIV-infected adults with HAART-related hypertriglyceridemia. Although no significant effect was noted on other metabolic abnormalities in this group of patients, l-carnitine may fulfill a role in the management of HAART-related hypertriglyceridemia. Data from this pilot work helped in the design of a randomized, comparative, multicentre trial, now in preparation. Acknowledgement The authors would like to thank Mr Ovid Da Silva for editing this manuscript. Maude Loignon Emil Toma

Time and feeding influences on cholesterol, triglyceride, glucose and insulin levels, and serum cholinesterase activity were assessed in a genetically-hyperlipidemic hyperphagic obese rat model, and compared with its lean litter-mate. Following a 28-day acclimation to a 12-hr light/dark cycle, blood samples were obtained every 2 hr from rats via tail bleed for a 24-hr period. Synchronization with other animal studies was established by endogenous serum cortisol levels [acrophase 18-20 hr after light onset (HALO) in both groups]. Triglycerides cholesterol, insulin and glucose levels were significantly elevated in obese versus lean rats. Obese rats were observed to feed throughout the 24-hr cycle, whereas lean litter-mates ate only during the dark cycle. No circadian rhythmicity was found in glucose levels with either rat group. Insulin levels were not correlated. Although triglyceride levels peaks at 13 HALO in lean rats, no pattern was observed in obese rats. Cholesterol levels were unchanged with time in either group. Cholinesterase activity followed a circadian rhythm in the lean, but not obese, rats with an acrophase estimated at 8 HALO. In contrast to previous reports, enzyme activity was not correlated with triglyceride levels in either rat group. Circadian similarities in insulin levels between rat groups suggest changes in insulin metabolism and/or secretion which are likely to be independent of feeding or activity. Conversely, triglyceride levels remained elevated throughout the 24-hr period in obese rats, whereas significant increases were observed in lean rats during the dark active cycle. These data suggest that triglyceride levels, and not insulin and cholesterol levels, are most likely dependent on feeding patterns.

Introduction: Knowledge about the relationship between Body Mass Index (BMI) and serum lipid levels is important in detecting the risk of cardiovascular diseases. The present study assessed the correlations of serum total cholesterol and triglyceride levels with BMI in a group of healthy undergraduates. Methods: A cross-sectional study was conducted among 104 students of the Faculty of Allied Health Sciences, University of Ruhuna. Serum total cholesterol and triglyceride levels of fasting blood samples were measured using enzymatic kits. Students’ heights and weights were measured, and BMI values were calculated. Information regarding students’ dietary habits, lifestyle and family history of diseases related to dyslipidemia was collected using a pre-tested and self-administered questionnaire. Data were analyzed using SPSS-20.0. Results: Mean (±SD) serum total cholesterol and triglyceride levels of the samples were 191.34±36.13 mg/dL and 116.25±59.9 mg/dL, respectively. The mean BMI was 22.48±3.59kg/m2. The total population had significant positive correlations between; BMI and total cholesterol level (r=0.23, p=0.017), and BMI and triglyceride level (r=0.42, p&lt;0.001). There was no significant correlation between BMI and cholesterol levels in male students (p=0.800) but, a significant positive correlation was found between triglyceride levels and BMI of them (p=0.017). Among female students, significant positive correlations with BMI were observed for both cholesterol (p=0.005) and triglyceride (p=0.002) levels. Family history of dyslipidemia related disease conditions showed a significant effect on the elevation of serum cholesterol and triglyceride levels of the students. Although there was no significant difference, the highest serum lipid levels were detected among students who consumed eggs more than once a day. Conclusions: Significant positive correlations were found between BMI and both serum total cholesterol and triglycerides levels in female students. Among the male students, there was a significant positive correlation between BMI and triglycerides, and no correlation between BMI and cholesterol levels.&#x0D; Keywords: Body mass index, Cholesterol, Correlation, Triglyceride, Undergraduates

Nephrotoxic effects caused by co-exposure to noise and toluene in New Zealand white rabbits: A biochemical and histopathological study

The development of lipodystrophy in HIV patients under highly active antiretroviral therapy (HAART) is an important problem associated with this therapy. Several authors have found inconclusive results when studying the metabolic mechanisms allied with those morphological changes [1–3]. In order to establish a possible association between changes in serum lipids and lipodystrophy we have investigated their evolution in HIV patients receiving HAART. Out of 297 HIV patients receiving HAART we selected 90 subjects in whom adherence to antiretroviral drugs was deemed adequate (more than 95% compliance). Follow-up included baseline and three monthly determinations of serum cholesterol and triglyceride levels. Lipodystrophy was diagnosed when the patient and doctor agreed on the presence of facial or limb lipoatrophy with or without increased deposits of fat in the abdomen or trunk. Patients were considered to have high cholesterol and triglyceride serum levels when their values were over 240 and 200 mg/dl, respectively. A total of 63.3% of the patients were men; the mean age was 38 years (range 21–64). Follow-up was 858 ± 215 days (range 364–1445). Overall, 62.8% of the patients showed lipid abnormalities: high triglyceride levels, 42%; high cholesterol levels 39%; high cholesterol and triglyceride levels, 24.2%. Triglyceride levels increased after 229 ± 144 days (range 35–825) and cholesterol levels increased after 248 ± 134 days (range 30–714) of starting HAART. Thirty-seven patients (40.7%) evolved to lipodystrophy after 488 ± 165 days (range 185–1084) of treatment. By the time lipodystrophy was diagnosed 79% of patients presented with hypertriglyceridemia (P = 0.0001) and 51.7% presented with hypercholesterolemia (NS). Table 1 shows that hypertriglyceridemia starting after 6 months of therapy was significantly associated with lipodystrophy. Multivariate analysis confirmed these findings (P = 0.0001).Table 1: Triglyceride and cholesterol levels (mg/dl) in patients with and without lipodystrophy. In the group with lipodystrophy, the number of patients with abnormally high triglyceride levels was progressively increasing during the time of observation: seven in month 3; 13 in month 6; 22 in month 12; and 24 in month 18. Eight patients with hypertriglyceridemia did not develop lipodystrophy. No differences were found between the lipodystrophy pattern or severity and the type of metabolic changes. The development of lipodystrophy has become the main problem associated with HAART. Several works have obtained different results when trying to establish a relationship between lipid alterations and morphological changes [1–6]. So, whereas some authors [4,5] found that metabolic changes consisting of high cholesterol or high triglyceride levels were more common in patients with lipodystrophy, others did not find such an association [6]. Our findings are consistent with a significant association between high triglyceride levels and lipodystrophy, and even suggest that the elevation of serum triglyceride levels may precede by several months the development of morphological changes. However, we have not been able to confirm any relationship between high triglyceride levels and the type or severity of lipodystrophy as other authors have found [3,5]. Consequently, we can conclude that an increase in triglyceride levels and the development of lipodystrophy followed a significant progressive and parallel course, and even that an increase in triglyceride levels could be considered to be a predictive marker of this event in many patients receiving HAART. Azucena Rodriguez-Guardado Jose Antonio Maradona Jose Antonio Carton Victor Asensi Acknowledgement The authors would like to thank Dr Enrique Fernández Bustillo for his statistical contribution.

Population mean levels of total cholesterol and fasting triglycerides have decreased substantially in the US in recent decades, but improvements in cardiometabolic health may have slowed among younger cohorts. Conversely, prevalence of diabetes (types 1 and 2) and obesity has increased, especially among adults younger than 65 years. It is unclear how trends in cholesterol, triglyceride, and glucose levels have changed across different birth cohorts and whether adverse trends in obesity are associated with these patterns. To quantify national trends in total cholesterol, fasting triglyceride, and fasting glucose levels among cohorts born between 1920 and 1999 and examine the potential association of these patterns with body mass index (BMI). This serial cross-sectional study used National Health and Nutrition Examination Survey (NHANES) data from the 1999-2000 to 2017-2020 cycles. Data were analyzed between November 1, 2023, and July 31, 2024. Participants included nonpregnant and noninstitutionalized US adults 18 years or older, born between 1920 and 1999, who had data collected from 1999 to 2020. Eight 10-year birth cohorts (from 1920 to 1999). Total cholesterol, fasting triglyceride, and fasting glucose levels and BMI. Quantile regression models reported average marginal effects to quantify mean change in cardiometabolic outcome measures per decade of birth years. Parametric regression models estimated the association of birth cohort with outcomes, assessing BMI as the mediator. Of 52 006 participants weighted to represent 264 664 915 US adults, weighted median age was 46 (IQR, 33-60) years and 50.6% were women. For the 50th percentile of measures, mean difference per 1-decade younger birth cohort was -7.1 (95% CI, -8.2 to -6.1) mg/dL for total cholesterol level, -13.1 (95% CI, -15.1 to -11.1) mg/dL for fasting triglyceride level, and 2.7 (95% CI, 2.3-3.1) mg/dL for fasting glucose level. BMI appeared to attenuate the associations between birth cohort and lipid levels and enhanced the associations between birth cohort and fasting glucose levels. However, up to 80% of the associations between birth cohorts and cardiometabolic outcomes were not mediated through BMI. In this cross-sectional study of 52 006 participants representing 264 664 915 US adults, population-level improvements in total cholesterol and triglyceride levels decelerated and adverse trends in glucose levels accelerated in more recent birth cohorts, which was partially mediated by concurrent increases in BMI. Public health initiatives that target antecedent health behaviors are needed to improve cardiometabolic health across generations.

We have used adenovirus-mediated gene transfer in apolipoprotein (apo)E(-/-) mice to elucidate the molecular etiology of a dominant form of type III hyperlipoproteinemia (HLP) caused by the R142C substitution in apoE4. It was found that low doses of adenovirus expressing apoE4 cleared cholesterol, whereas comparable doses of apoE4[R142C] greatly increased plasma cholesterol, triglyceride, and apoE levels, caused accumulation of apoE in VLDL/IDL/LDL region, and promoted the formation of discoidal HDL. Co-expression of apoE4[R142C] with lecithin cholesterol acyltransferase (LCAT) or lipoprotein lipase (LPL) in apoE(-/-) mice partially corrected the apoE4[R142C]-induced dyslipidemia. High doses of C-terminally truncated apoE4[R142C]-202 partially cleared cholesterol in apoE(-/-) mice and promoted formation of discoidal HDL. The findings establish that apoE4[R142C] causes accumulation of apoE in VLDL/IDL/LDL region and affects in vivo the activity of LCAT and LPL, the maturation of HDL, and the clearance of triglyceride-rich lipoproteins. The prevention of apoE4[R142C]-induced dyslipidemia by deletion of the 203-299 residues suggests that, in the full-length protein, the R142C substitution may have altered the conformation of apoE bound to VLDL/IDL/LDL in ways that prevent triglyceride hydrolysis, cholesterol esterification, and receptor-mediated clearance in vivo.

The effects of deltamethrin on some serum biochemical parameters in mice

This study designed to determine the effect of vitamine E and sodium selenite on the level of some biochemical parameters in serum of male rats exposed to oxidative stress induced by cadmium chloride. The study showed that treatment with cadmium chloride (25 mg/liter of drinking water) for 30 days caused a significant decrease in the body weight, with a significant increase in the level of glucose, cholesterol and triglycerides. Treatment of rats exposed to oxidative stress induced by cadmium chloride with vitamin E (500 mg/kg body weight) for 30 days show a non significant change in the body weight, but there was a significant increase in the level of glucose, cholesterol and triglycerides. Moreover treated rats exposed to oxidative stress induced by cadmium chloride (25 mg/liter drinking water) together with sodium selenite (0.5 mg/kg diet) for 30 days showed a non significant changes in body weight and the level of triglyceride, but a significant decrease in levels of glucose & cholesterol. Treatment with vitamin E together with sodium selenite to rats exposed to oxidative stress induced by cadmium chloride for 30 days showed a significant decrease in the level of glucose, cholesterol and triglycerides. It was concluded that administration of vitamin E with sodium selenite as antioxidants produced a significant decrease in glucose, cholesterol and triglycerides levels in rats exposed to oxidative stress induced by cadmium chloride.

Objective: To study the variations and influencing factors of serum triglycerides and cholesterol levels during pregnancy and postpartum. Methods: A retrospective study was performed among 5 020 healthy singleton (95.10%, 4 774/5 020) and twin (4.90%, 246/5 020) women who had delivery in Women's Hospital, Zhejiang University School of Medicine from January 2011 to December 2016. Serum triglycerides and cholesterol levels during pregnancy and postpartum of all the cases were collected. Both singleton and twin pregnant women were divided into advanced age and appropriate age groups, and then data of serum sample were assigned to 3 groups according to the gestation weeks, which were second trimester pregnancy (24-28 gestation weeks) , third trimester pregnancy (32-41 gestation weeks) and postpartum (within 72 hours after delivery) . The serum triglycerides and cholesterol levels in each groups were compared. Results: (1) Serum triglycerides and cholesterol levels during the second trimester pregnancy, third trimester pregnancy and postpartum were higher than levels of non-pregnancy in both singleton and twin groups (all P<0.05) . (2) Serum triglycerides and cholesterol levels in the third trimester pregnancy group were higher than those of second trimester pregnancy group in both advanced age and appropriate aged women regardless singleton or twin pregnancy (all P<0.05) . The 95%CI of serum lipid levels in each group during second and third trimester pregnancy were as follows: in appropriate aged singleton group, the triglycerides levels were 1.07-4.13 and 1.52-7.21 mmol/L, and the cholesterol levels were 2.77-12.11 and 4.44-9.36 mmol/L. In advanced aged singleton group, the triglycerides levels were 1.28-4.61 and 1.70-7.80 mmol/L, and the cholesterol levels were 4.35-8.40 and 4.46-9.35 mmol/L; in appropriate aged twin group, the triglycerides levels were 1.39-7.16 and 1.90-9.29 mmol/L, and the cholesterol levels were 4.99-12.16 and 4.52-10.07 mmol/L; in advanced aged twin group, the triglycerides levels were 1.61-5.32 and 1.94-9.29 mmol/L, and the cholesterol levels were 5.24-8.10 and 4.53-8.86 mmol/L. (3) Serum lipids levels rapidly decreased during postpartum compared to the third trimester pregnancy. The 95%CI of blood lipid levels in each group were as follows: in appropriate aged singleton group, the triglycerides level was 0.90-5.64 mmol/L and the cholesterol level was 4.70-8.52 mmol/L; in advanced aged singleton group, the triglycerides level was 0.87-5.43 mmol/L and the cholesterol level was 4.68-9.04 mmol/L; in appropriate aged twin group, the triglycerides level was 1.20-8.21 mmol/L and the cholesterol level was 4.66-8.45 mmol/L; in advanced aged twin group, the triglycerides level was 1.32-6.61 mmol/L, and the cholesterol level was 5.01-7.94 mmol/L. (4) Serum triglycerides and cholesterol levels in twin pregnant women were significantly higher than in singleton during the second trimester and third trimester pregnancy both in advanced age and appropriate age groups (all P<0.05) . During postpartum, there was no difference in serum lipid levels between the singleton and twin pregnant women in appropriate age group (triglycerides: P=0.982; cholesterol: P=0.759, respectively) . While the serum lipid levels in twin pregnant women were significantly higher than those of singleton women in advanced age group (triglycerides: P=0.000; cholesterol: P=0.000, respectively) . Conclusions: The standard of serum lipid levels of non-pregnant adults is not suitable for assessing that in pregnant women. Regardless of singleton or twin pregnancy, serum triglyceride and cholesterol levels during pregnancy elevate with the increasing gestational week and then rapidly decrease during postpartum. Age and twins are the influencing factors of the elevated physiological lipid levels during pregnancy.

We conducted a genome-wide scan using variance components linkage analysis to localize quantitative-trait loci (QTLs) influencing triglyceride (TG), high density lipoprotein-cholesterol (HDL-C), low density lipoprotein-cholesterol, and total cholesterol (TC) levels in 3,071 subjects from 459 families with atherogenic dyslipidemia. The most significant evidence for linkage to TG levels was found in a subset of Turkish families at 11q22 [logarithm of the odds ratio (LOD)=3.34] and at 17q12 (LOD=3.44). We performed sequential oligogenic linkage analysis to examine whether multiple QTLs jointly influence TG levels in the Turkish families. These analyses revealed loci at 20q13 that showed strong epistatic effects with 11q22 (conditional LOD=3.15) and at 7q36 that showed strong epistatic effects with 17q12 (conditional LOD=3.21). We also found linkage on the 8p21 region for TG in the entire group of families (LOD=3.08). For HDL-C levels, evidence of linkage was identified on chromosome 15 in the Turkish families (LOD=3.05) and on chromosome 5 in the entire group of families (LOD=2.83). Linkage to QTLs for TC was found at 8p23 in the entire group of families (LOD=4.05) and at 5q13 in a subset of Turkish and Mediterranean families (LOD=3.72). These QTLs provide important clues for the further investigation of genes responsible for these complex lipid phenotypes. These data also indicate that a large proportion of the variance of TG levels in the Turkish population is explained by the interaction of multiple genetic loci.

Adjunctive fluvoxamine inhibits clozapine metabolism and decreases plasma norclozapine (a toxic metabolite of clozapine) to clozapine ratios. This study aimed to demonstrate the effects of fluvoxamine on clozapine-related weight gain, hyperglycemia, and lipid abnormalities. Sixty-eight treatment-resistant inpatients with a DSM-IV diagnosis of schizophrenia were randomly assigned to 2 treatment groups for 12 weeks. The monotherapy group (N = 34) received clozapine (< or = 600 mg/day). The coadministration group (N = 34) received fluvoxamine (50 mg/day) plus low-dose clozapine (< or = 250 mg/day). The study was conducted from August 1999 to October 2002. The 2 groups were similar in demographic data; baseline body weight and body mass index (BMI); baseline serum glucose, triglyceride, and cholesterol levels; and steady-state plasma clozapine concentration. The monotherapy patients (but not the coadministration patients) had significantly higher (p < .05) body weight, BMI, and serum glucose and triglyceride levels after treatment than at baseline. At week 12, the monotherapy patients also had significantly higher glucose (p = .035), triglyceride (p = .041), and norclozapine (p = .009) (and numerically higher cholesterol) levels than the cotreatment patients. The changes in weight and serum glucose and triglyceride levels were significantly correlated (p = .026, p = .005, and p = .028, respectively) with the plasma concentration of norclozapine but not with plasma levels of clozapine. These results suggest that fluvoxamine cotreatment can attenuate weight gain and metabolic disturbances in clozapine-treated patients. Plasma levels of norclozapine, but not clozapine, are associated with increases in weight and serum glucose and triglyceride levels. Of note, coadministration of fluvoxamine could increase plasma clozapine levels markedly and carry the risk of adverse events. If this combined treatment is applied, conservative introduction with reduced clozapine dosage and careful therapeutic drug monitoring of clozapine concentration is recommended.

Insulin sensitivity is changed during the neonatal period in small for gestational age (SGA) infants. Yet, the interventional strategies are still limited. We aimed to investigate the effects of supplementation with high folate and vitamin B12 diets in the early postnatal period on the changes in insulin sensitivity in an intrauterine growth retardation (IUGR) rat model. IUGR rat model was established by both low-protein diet feeding and daily diet restriction. High folate and vitamin B12 diet was supplied in IUGR as nutritional interventional group (IUGR-I), otherwise, the non-intervened IUGR group (IUGR-NI). In this study, male rats were studied in order to avoid hormonal and gender influence. At 21, 60 and 120 days, fasting plasma glucose, insulin, triglyceride, cholesterol, and homocysteine levels were measured among the control, IUGR-I, and IUGR-NI groups. Pearson analysis was used to evaluate the correlation between homocysteine and fasting blood glucose, insulin, HOMA-IR, triglyceride, and cholesterol levels. We established IUGR rat model by both low protein and restricted diet feeding during pregnancy and the incidence of IUGR pups was 93.33%. There was no difference in fasting glucose, insulin, HOMA-IR, triglyceride and cholesterol levels between the control, the IUGR-NI and the IUGR-I group at day 21. At day 60, insulin, HOMA-IR and triglyceride levels in the IUGR-I group were remarkably lower than those in the IUGR-NI group, but still higher than those in the control group (F=38.34, P=0.02; F=49.48, P=0.02; F=17.93, P<0.001, respectively). At day 120, glucose, insulin, HOMA-IR and Hcy levels in the IUGR-I group were obviously lower than those in the IUGR-NI group, although still higher than those in the control group (F=21.60, P<0.001; F=164.46, P<0.001; F=75.15, P<0.001; F=35.46, P<0.001, respectively). There were no significant differences in triglyceride and cholesterol levels between the IUGR-I group and the control group at day 120. At 120-day, homocysteine in IUGR-I group was highly positively correlated with fasting glucose and HOMA-IR (r=0.863, P=0.006; r=0.725, P=0.042, respectively); Only homocysteine was positively correlated with fasting glucose in IUGR-NI group (r=0.721, P=0.044). Early supplementation of folate and vitamin B12 improved insulin resistance and lipid levels in IUGR rats to some extent, along with decreasing homocysteine levels, but not enough to completely repair glucose and lipid metabolism.

The present research study was designed to evaluate the effect of zinc supplementation on body weight, serum triglyceride, cholesterol, glucose homeostasis, oxidative stress, and hepatic function in mice. Mice were treated with zinc sulphate at an equivalent weight of 6.5 mg/kg-body weight elemental zinc for four weeks. Bodyweight, serum glucose, triglyceride, cholesterol, serum MDA, nitric oxide, vitamin C, and hepatic enzymes level were determined at the end of the study period. Data from this study showed that supplementation with zinc in mice maintained a balanced blood glucose homeostasis throughout the experimental period. Moreover, treatment with zinc showed a significant (p &lt;0.05) decrease in serum triglyceride and cholesterol level along with a decrease in the body weight compared to control. Treatment with zinc significantly attenuated the rate of lipid peroxidation whereas increased the level of vitamin C and NO level. The protective effect of zinc on liver activity was observed. Treatment with zinc showed a strong negative association with serum total cholesterol (r= -0.934, p = 0.02), triglycerides level (r= -0.709, p = 0.05), and body weight (r= -0.899, p = 0.01). The present findings demonstrate that zinc supplementation can be helpful to maintain a glucose homeostasis, ameliorate hyperlipidemia, oxidative stress, and liver dysfunction. Therefore, zinc supplementation can be suggested to alleviate diseases associated with metabolic syndrome and oxidative stress.&#x0D; Dhaka Univ. J. Pharm. Sci. 20(1): 59-66, 2021 (June)

SUMMARY The objective of our experiment was to determine th e utilization protocol of enzymatic preparations in concordance with the wheat and barl ey proportion in the combined forages for broiler chickens and the effect exerted by them on sanguine indices. The experiment was performed during six weeks, on a number of 150 chickens, distributed in five experimental groups (LE1, LE2 and LE3, LE4, LE5), as follows: the experimental group LE1, fed with forage without wheat in its structure, the experime ntal group LE2, fed with combined forage including wheat in proportion of 60%, the experimental group LE3, fed with forage including 60 % wheat, with addition of 100 ppm xylanase, the experimental group LE4, with 30% wheat and barley in the same proportion, and the ex perimental group LE5, fed with wheat and barley like LE4 and with addition of 50 ppm xylanas e and 50 ppm beta glucanase. At the age of 6 weeks, successive to chicken killing, we sampl ed the blood and determined its content in cholesterol and triglycerides. Successive to our de terminations, we could observe that the triglyceride level in LE2 was smaller with 17.76% t han in LE1, and the cholesterol level was bigger with 4.26%, when compared with the same group. The addition of the wheat-specific enzyme in the case of LE3 does not cause major changes of the triglyceride (1.43%) and cholesterol (0.9%) levels. Wheat substitution with barley determines changes of the triglyceride and cholesterol levels; the triglyceri des increase with 33.81%, and the cholesterol with 16.36%. In LE5, the supplementation with the t wo enzymes specific to wheat- and barley- NSP determines a slight increase of the tri glyceride level, with 1.07%, and of cholesterol with 6.64%. LE4 and LE5 represent exceptions, because cholesterol levels correspond to the limits mentioned by the literatur e of specialty. Consequently, we may draw the conclusion that wheat utilization in a big prop ortion, respectively 60% of forage structure, determines a decrease of the triglyceride level (17 .24%) and a slight increase of the cholesterol level (4.26 %). The enzyme supplementation does not change the level of these sanguine constants. The relationships between visco sity, nutrient absorption and plasmatic cholesterol require further studies, with various p olysaccharide sources. REFERENCES